Inhibition of human platelet functions by verapamil.
The effects of verapamil, a coronary vasodilator, on platelet functions was studied. Platelet aggregation induced by ADP, epinephrine or collagen was inhibited by verapamil in vitro. Calcium ionophore A23187-induced platelet aggregation was also inhibited by verapamil in a concentration dependent manner. In washed platelets, verapamil caused a dose-dependent inhibition of serotonin release induced either by thrombin or A23187 in the absence of extracellular calcium. Addition of 1 mM CaCl2 with A23187 or thrombin partially overcame this inhibition. Addition of 1 mM CaCl2 in the absence of verapamil had no effect on thrombin- or A23187-induced secretion. When verapamil was administered to the healthy volunteers at the dosage commonly used, inhibition of platelet aggregation was observed 2 hrs after the drug ingestion. It is of great interest that verapamil potentiated the anti-aggregating activity of prostacyclin in vitro. Our results may suggest a potential role for verapamil in the treatment of thrombotic disorders.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects*; D000001:Calcimycin / Q000494:pharmacology; D003094:Collagen / Q000494:pharmacology; D004357:Drug Synergism; D004837:Epinephrine / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D012701:Serotonin / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology*
D012701:Serotonin; D000001:Calcimycin; D000244:Adenosine Diphosphate; D003094:Collagen; D014700:Verapamil; D011464:Epoprostenol; D004837:Epinephrine